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外源性应激源对皮肤清道夫受体 B1 水平的调节可损害“体外”伤口闭合。

Modulation of cutaneous scavenger receptor B1 levels by exogenous stressors impairs "in vitro" wound closure.

机构信息

Dept. of Life Sciences and Biotechnology, University of Ferrara, Ferrara, Italy.

Department of Medical, Surgery and Neurosciences, University of Siena, Siena, Italy.

出版信息

Mech Ageing Dev. 2018 Jun;172:78-85. doi: 10.1016/j.mad.2017.11.006. Epub 2017 Nov 1.

DOI:10.1016/j.mad.2017.11.006
PMID:29102450
Abstract

Scavenger receptor B1 (SR-B1) is a trans-membrane protein, involved in tissue reverse cholesterol transport. Several studies have demonstrated that SR-B1 is also implicated in other physiological processes, such as bacteria and apoptotic cells recognition and regulation of intracellular tocopherol and carotenoids levels. Among the tissues where it is localized, SR-B1 has been shown to be significantly expressed in human epidermis. Our group has demonstrated that SR-B1 levels are down-regulated in human cultured keratinocytes by environmental stressors, such as cigarette smoke, via cellular redox imbalance. Our present study aimed to investigate whether such down-regulation was confirmed in a 3D skin model and under other environmental challengers such as particulate matter and ozone. We also investigated the association between oxidation-induced SR-B1 modulation and impaired wound closure. The data obtained showed that not only cigarette, but also the other environmental stressors reduced SR-B1 expression in epidermal cutaneous tissues and that this effect might be involved in impaired wound healing.

摘要

清道夫受体 B1(SR-B1)是一种跨膜蛋白,参与组织逆向胆固醇转运。多项研究表明,SR-B1 还与其他生理过程有关,如细菌和凋亡细胞的识别,以及细胞内维生素 E 和类胡萝卜素水平的调节。在其定位的组织中,已经表明 SR-B1 在人表皮中表达显著。我们的研究小组已经证明,环境应激物,如香烟烟雾,通过细胞氧化还原失衡,下调人培养角质形成细胞中的 SR-B1 水平。本研究旨在探讨这种下调是否在 3D 皮肤模型中得到证实,以及在其他环境挑战物如颗粒物和臭氧下是否得到证实。我们还研究了氧化诱导的 SR-B1 调节与伤口闭合受损之间的关联。获得的数据表明,不仅香烟,而且其他环境应激物也降低了表皮皮肤组织中的 SR-B1 表达,而这种作用可能与伤口愈合受损有关。

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